The proposed work will expand ongoing investigations of the pressor and water-ingestion effects of central nervous system administration of angiotensin II. Recent evidence (Hoffman and Phillips, 1976) indicates that rostral third ventricular structures mediate the pressor and drinking effects of angiotensin II (A II). Pilot work indicating that A II-induced pressor activity emanates from the subfornical organ (SFO) will be expanded to include investigations of other rostral third-ventricular structures, particularly the organum vasculosum of the lamina terminalis (OVLT). Several mutually confirmatory techniques, such as intracranial injection, pharmacologic blockade, lesions, and ventricular plugging, will be used to determine the most effective site of pressor action of A II. The possibility of an SFO pressor effect caused by cholinomimetics will also be evaluated. By understanding the possible pressor function of two structures (SFO and OVLT) which lack the blood-brain barrier, significant progress may be made in our understanding of the role of circulating antgiotensin II in some forms of hypertension.